Angiotensin II increases and decreases arterial pressure by acting at angiotensin type 1 and type 2 receptors respectively. Renovascular hypertensive rats exhibit a high level of activity of the peripheral and central renin-angiotensin system. Therefore, in the present study we evaluated the effect of increasing the expression of angiotensin type 2 receptors in the solitary-vagal complex [nucleus of the solitary tract/dorsal motor nucleus of the vagus], a key brainstem region for cardiovascular regulation, on the development of renovascular hypertension. Holtzman normotensive rats were implanted with a silver clip around the left renal artery to induce 2 kidney-1 clip renovascular hypertension. Three weeks later, rats were microinjected in the solitary-vagal complex with either an adeno-associated virus to increase the expression of angiotensin type 2 receptors, or with a control vector. We observed that increasing angiotensin type 2 receptor expression in the solitary-vagal complex attenuated the development of renovascular hypertension and also reversed the impairment of the baroreflex and the increase in the low frequency component of systolic blood pressure observed in renovascular hypertensive rats. Further, an observed decrease in mRNA levels of angiotensin converting enzyme 2 in the solitary-vagal complex of renovascular hypertensive rats was restored to control levels following viral-mediated increases in angiotensin type 2 receptors at this site. Collectively, these data demonstrate specific and beneficial effects of angiotensin type 2 receptors via the brain of hypertensive rats, and suggest that central angiotensin type 2 receptors may be a potential target for therapeutics in renovascular hypertension.

The nucleus of the solitary tract (NTS) is the primary site of visceral afferents to the central nervous system. In the present study, we investigated the effects of lesions in the commissural portion of the NTS (commNTS) on the activity of vasopressinergic neurons in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, plasma vasopressin, arterial pressure, water intake, and sodium excretion in rats with plasma hyperosmolality produced by intragastric 2 M NaCl (2 ml/rat). Male Holtzman rats with 15-20 days of sham or electrolytic lesion (1 mA; 10 s) of the commNTS were used. CommNTS lesions enhanced a 2 M NaCl intragastrically induced increase in the number of vasopressinergic neurons expressing c-Fos in the PVN (28 ± 1, vs. sham: 22 ± 2 c-Fos/AVP cells) and SON (26 ± 4, vs. sham: 11 ± 1 c-Fos/AVP cells), plasma vasopressin levels (21 ± 8, vs. sham: 6.6 ± 1.3 pg/ml), pressor responses (25 ± 7 mmHg, vs. sham: 7 ± 2 mmHg), water intake (17.5 ± 0.8, vs. sham: 11.2 ± 1.8 ml/2 h), and natriuresis (4.9 ± 0.8, vs. sham: 1.4 ± 0.3 meq/1 h). The pretreatment with vasopressin antagonist abolished the pressor response to intragastric 2 M NaCl in commNTS-lesioned rats (8 ± 2.4 mmHg at 10 min), suggesting that this response is dependent on vasopressin secretion. The results suggest that inhibitory mechanisms dependent on commNTS act to limit or counterbalance behavioral, hormonal, cardiovascular, and renal responses to an acute increase in plasma osmolality.

Resumo: a obesidade comumente é associada com outras doenças como: hipertensão arterial, diabetes mellitus tipo II, cardiovasculares e inflamação crônica. Estudos demonstram o tecido adiposo (TA) como um órgão endócrino capaz de influenciar a homeostase energética e hemodinâmica, além de ter papel importante na resposta inflamatória. O termo adipocina é utilizado para nomear peptídeos bioativos sintetizados e secretados por adipócitos. O interesse em estudar essas proteínas teve início com a descoberta da leptina e suas diversas funções, hoje já sabemos que o TA secreta outros hormônios, proteínas de fase aguda, quimiocinas, fatores hemostáticos e hemodinâmicos e fatores de crescimento. Este trabalho teve por objetivo estudar os principais grupos de adipocinas visando uma maior compreensão de seus mecanismos de ação, das finalidades e influências no desenvolvimento da obesidade e estado de inflamação crônica. Foi observado que essas adipocinas em desequilíbrio promovem impacto em diversas funções corporais, alterando a ingesta alimentar, sensibilidade à insulina, resposta imune, angiogênese, pressão arterial, metabolismo lipídico e balanço energético. Dessa maneira se faz necessária uma compreensão dos efeitos do tratamento como atividade física, nutrição, aspecto psicológico e clínica sobre o controle hormonal e de citocinas, a fim de se desenvolver terapias mais eficazes, diminuindo as complicações da obesidade. Palavras-chave: Adipocinas. Leptina. Adiponectina. Resistina. Obesidade.Abstract: the obesity is commonly associated with other diseases such as hypertension, diabetes mellitus type II, cardiovascular and chronic inflammation. Studies revealed adipose tissue (AT) as an endocrine organ capable of influencing the energy and hemodynamic homeostasis, and play an important role in the inflammatory response. The adipokine term is used to name bioactive peptides synthesized and secreted by adipocytes. The interest in studying these proteins began with the discovery of leptin and its various functions, today we know that the TA secret other hormones, acute phase proteins, chemokines, hemostatic and hemodynamic factors and growth factors. This study aims to investigate the major adipokines groups seeking a greater understanding of their mechanisms of action, its purposes and influences the development of obesity and chronic state of inflammation. It was observed that these imbalance adipokines have a impact on several body functions, altering dietary intake, insulin sensitivity, immune response, angiogenesis, blood pressure, lipid metabolism and energy. Thus, a understanding of the effects of treatment such as physical activity, nutrition, psychological and clinical aspects on hormonal and cytokine control is necessary in order to develop more effective therapies, reducing the complications of obesity.

These results indicate that an increased expression of MIF within the nucleus of the solitary tract neurons of SHRs lowers blood pressure and restores baroreflex function.